Comparative genomic hybridization of Candida albicans and Candida dublinienis
Ontology highlight
ABSTRACT:
ORGANISM(S): Candida albicans
SUBMITTER: David Coleman
PROVIDER: E-MEXP-99 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Publications
Comparative genomics using Candida albicans DNA microarrays reveals absence and divergence of virulence-associated genes in Candida dubliniensis.
Moran Gary G Stokes Cheryl C Thewes Sascha S Hube Bernhard B Coleman David C DC Sullivan Derek D
Microbiology (Reading, England) 20041001 Pt 10
Candida dubliniensis is a pathogenic yeast species closely related to Candida albicans. However, it is less frequently associated with human disease and displays reduced virulence in animal models of infection. Here comparative genomic hybridization was used in order to assess why C. dubliniensis is apparently less virulent than C. albicans. In these experiments the genomes of the two species were compared by co-hybridizing C. albicans microarrays with fluorescently labelled C. albicans and C. d ...[more]
Similar Datasets
Project description:22 plexiform neurofibromas from 18 unrelated neurofibromatosis-type 1 patients were screened with a high resolution array-CGH. Each PNF DNA (somatic tumor DNA) was individually hybridized on Agilent whole human genome 244K microarrays (Platform GPL4091) using the matched genomic constitutional DNA (lymphocytes DNA) from the corresponding patient as reference, in order to detect tumor-specific aberrations. NF1-associated plexiform neurofibromas DNA vs. constitutional DNA
2011-09-29 | E-GEOD-24328 | biostudies-arrayexpress
Project description:To allow acute characterization of ABCB4 locus constitutional deletion in two patients with cholelithiasis/cholestasis, an Agilent 2X400 array CGH was used. Goal was to obtain genomic rearrangements fine characterization in order to describe ABCB4 constitutional deletions. ABCB4 locus microdeletions characterization vs reference sample (pool of six normal control DNAs)
2011-10-04 | E-GEOD-28676 | biostudies-arrayexpress
Project description:To allow accute charaterization of NF1 locus constitutional microdeletion in 70 NF1 patients, a custom array CGH was developped. Goal was to obtain genomic rearrangements fine characterization in order to perform genotype-phenotype correlation in NF1 microdeleted patients. To serve as a reference group in our genotype-phenotype correlation study in NF1 microdeletion patients, non-deleted NF1 patients (i.e. patients with an intragenic NF1 mutation) were also selected from our database. A total of 389 NF1 patients were included in the reference group of non-deleted patients. Multiple logistic regression was performed to test the association of each clinical feature individually with the type of constitutional NF1 mutation (intragenic mutation vs. microdeletion). The phenotypic traits of the 389 reference patients are available in the "GSE19730_control_patient_characteristics.txt" supplementary file on the Series record. NF1 locus microdeletions characterization vs reference sample (pool of six normal control DNAs)
2010-05-26 | E-GEOD-19730 | biostudies-arrayexpress
Project description:Male factor infertility affects about 7% of men in the general population and it can be related to a number of different etiologic factors, including genetic anomalies. Both sex chromosomes are enriched in genes prevalently or exclusively expressed in the testis. Nevertheless only the Y chromosome-linked Copy Number Variants (CNVs) and Y-linked genes have been demonstrated as important contributors to impaired sperm production in humans Data on the potential role of X-linked gene products in spermatogenesis derives mainly from model organisms. X-linked genes seem to be expressed both in pre-meiotic and post-meiotic germ cells in the mouse testis and interestingly those expressed in the post-meiotic cells belong to multicopy gene families. The apparent paucity of X-linked factors in male infertility is most likely related to the scarcity of studies, which focused only on a total of seven genes. No pathogenic mutations causing infertility have, thus far, been described in these genes, with the exception of AR gene In order to advance in the understanding of the role of X-linked CNVs and genes in male infertility, we applied an innovative approach based on high resolution X chromosome specific CGH array. Given that such a detailed analysis of the X chromosome has not been published so far and the testicular function of subjects included in the Genomic Variant Database is unknown (except for 24 X-linked CNVs reported in the recent paper by Tuttelmann), our is the first study providing a detailed analysis of X-linked losses and gains in several hundreds of subjects with known sperm parameters. The study was approved by the local Ethical Committees of the University Hospital Careggi (Italy) and the Fundacio Puigvert (Spain). All participants signed an informed consent. 96 infertile subjects with different grade of spermatogenic impairment (74 azoospermic, 6 mild oligozoospermia and 16 severe oligozoospermic men) and 103 normozoospermic men have been analyzed with aCGH. All known causes of impaired spermatogenesis have been excluded in the patients and testis histology was available for 47 men. The ethnic composition was similar in the controls and patients groups (40% Spanish and 60% Italians). A customized array-CGH platform (custom 8 x 60K, Agilent Technologies) was generated using the eArray software (http://earray.chem.agilent.com/); probes, selected from those available in the Agilent database, covered the whole X chromosome, including Xp and Xq pseudoregions, with an average resolution of 4 Kb. As a reference DNA, we used the same normozoospermic subject for the entire study population. This control DNA was already characterized for CNV content in previous array-CGH experiments against different (8) normospermic controls. In the second part of the study, we performed a case-control study on 31 selected CNVs which appeared to be specific for infertile men after the aCGH analysis. For these selected losses a total of 359 patients and 370 normozoospermic controls were studied. With regard to the gains, 270 patients and 325 controls were analyzed (further phenotypic data are provided in supplementary tables 1a-e). Deletions were analyzed by PCR plus/minus, whereas loss 31 and all the gains have been analyzed with Real Time PCR using TaqMan Copy Number Assay. CNV code Loss or Gain Region Size (kb) Start End 1a GAIN Xp22.33 224,83 1544 226372 4.A GAIN Xp22.33 237,08 153373 390452 5 GAIN Xp22.33 160,10 302644 462740 5.A GAIN Xp22.33 241,98 674222 916206 5.B LOSS Xp22.33 12,63 701071 713696 5.C GAIN Xp22.33 420,72 747358 1168080 11 GAIN Xp22.33 39,73 1347599 1387328 12 GAIN Xp22.33 17,30 1693897 1711194 12.A GAIN Xp22.33 6,61 1693897 1700511 12.B GAIN Xp22.33 683,74 1716023 2399766 14 GAIN Xp22.33 1,40 1896197 1897608 15 LOSS Xp22.33 1,40 1896197 1897608 15.A GAIN Xp22.33 27,94 2382699 2410643 15.B GAIN Xp22.33/22.32 280,09 4206493 4486580 16 LOSS Xp22.32 7,76 4250413 4258174 16.A GAIN Xp22.31 1609,42 6487238 8096662 17 LOSS Xp22.31 31,70 6594834 6626533 18 LOSS Xp22.31 82,00 6756310 6838310 19 GAIN Xp22.31 245,03 7002649 7247676 19.A GAIN Xp22.31 129,96 7961788 8091751 19.B GAIN Xp22.31 177,54 8411159 8588699 20 GAIN Xp22.2 602,10 11104518 11706614 20.A GAIN Xp22.2 665,88 14590604 15256487 20.B GAIN Xp22.13 13,34 18018894 18032238 22 LOSS Xp22.11 24,35 22969648 22993997 23 LOSS Xp21.3 6,69 25274024 25280712 24 LOSS Xp21.3 67,33 26891769 26959101 25 GAIN Xp21.3 60,40 27277529 27337933 25.A LOSS Xp21.2 9,69 31282923 31292613 25.B LOSS Xp21.1 28,26 33953232 33981492 25.C GAIN Xp21.1 185,02 34931807 35116827 25.D GAIN Xp21.1 215,00 35269628 35484626 26 GAIN Xp21.1 88,57 37168387 37256960 27 GAIN Xp21.1 9,61 37242364 37251969 30 GAIN Xp11.3 81,13 47766391 47847516 31 LOSS Xp11.3 81,13 47766391 47847516 31.A GAIN Xp11.23 78,87 48021982 48100848 32 LOSS Xp11.22 4,15 52065798 52069943 33.A LOSS Xp11.21 58,89 56403390 56462278 34.A GAIN Xp11.12 48,06 56870427 56918489 35 GAIN Xp11.1 117,14 57318438 57435573 36.A GAIN Xq11 716,03 63925948 64641977 38 GAIN Xq13.2 8,98 72202996 72211976 38.A GAIN Xq13.2 192,04 74375875 74567915 38.B GAIN Xq13.3 153,23 75123387 75276621 39 GAIN Xq21.1 21,98 76992067 77014050 40 GAIN Xq21.1 5,28 80112246 80117526 49 GAIN Xq22.1 5,30 100942190 100947490 50 LOSS Xq22.1 45,36 101803578 101848935 51 GAIN Xq22.2 34,69 103152319 103187013 53.A LOSS Xq24 170,73 118278913 118449646 54 LOSS Xq24 44,85 118281024 118325874 55 GAIN Xq24 206,90 118691020 118897917 55.A GAIN Xq25 53,80 120385787 120439584 56 LOSS Xq25 86,07 124632886 124718959 57 LOSS Xq25 188,03 124929673 125117699 58 GAIN Xq25 9,68 125143278 125152957 58.A LOSS Xq25 12,68 125198109 125210792 59.A GAIN Xq26.3 24,69 134151039 134175725 60 GAIN Xq26.3 42,30 134585636 134627936 60.A LOSS Xq26.3 50,84 134801361 134852198 60.B GAIN Xq26.3 13,45 136050422 136063872 60.C GAIN Xq26.3 91,26 137089527 137180783 60.D LOSS Xq27.1 217,83 140175103 140392930 61 LOSS Xq27.2 4,67 140773893 140778561 64 LOSS Xq27.3 3,92 143436347 143440268 66 LOSS Xq27.3 7,35 145030566 145037917 66.A LOSS Xq28 37,12 147393583 147430698 67 LOSS Xq28 5,42 148456474 148461889 68 GAIN Xq28 105,66 148686631 148792286 69 LOSS Xq28 11,77 154044877 154056645 71 LOSS Xq28 290,99 154586913 154877901 71.A LOSS Xq28 122,36 154755542 154877901
2012-10-01 | E-GEOD-37948 | biostudies-arrayexpress
Project description:Sexual development in mammals is based on a complicated and delicate network of genes and hormones that have to collaborate in a precise manner. The dark side of this pathway is represented by pathological conditions, wherein sexual development does not occur properly either in the XX and the XY background. Among them a conundrum is represented by the XX individuals with at least a partial testis differentiation even in absence of SRY. This particular condition is present in various mammals including the dog. Seven dogs characterized by XX karyotype, absence of SRY gene and testicular tissue development were analysed by Array-CGH. In two cases the array-CGH analysis detected an interstitial heterozygous duplication of chromosome 9. The duplication contained the SOX9 coding region.In this work we provide for the first time a causative mutation for the XXSR condition in the dog. Moreover this report supports the idea that the dog represents a good animal model for the study of XXSR condition caused by abnormalities in the SOX9 locus. Seven dogs from different breeds have been considered in this study. All clinical activities and surgical experiments on the dogs were carried out following the Federation of European Laboratory Animal Science AssociationM-bM-^@M-^Ys recommendations and European Union legislation (Council Directive 86/609/EEC). During the research no animals were sacrificed. Array-CGH was performed using a custom Agilent Canine Genome CGH Microarray 180 K (Agilent Technologies, Santa Clara, California, USA) and processed according to the manufacturerM-bM-^@M-^Ys protocol. The arrays were analyzed with the Agilent scanner and the Feature Extraction software (v10.7.3.1). A graphical overview was obtained using the CGH analytics software (v7.0.4.0). The DNA extracted from a normal female (boxer breed) was used as the control in all cases. Sox9 duplications detected by array CGH were confirmed by Real-Time-qPCR .
2014-08-05 | E-GEOD-57137 | biostudies-arrayexpress
Project description:In a study to elucidate the genetic defects in patients with X-linked intellectual disability (XLID) we performed X chromosome-specific BAC-array-CGH and identified 0.33 to 1.0 Mb nonrecurrent copy number gains at Xp11.22 in affected males of unrelated XLID families. All aberrations segregate with the disease in the families and the carrier mothers show a nonrandom X-inactivation. Affected males suffered from mild to moderate ID. Tiling Xp11.22 region-specific oligo-array (ChrX:52.50 - 54.50 Mb) revealed that all aberrations had different start and stop sites. The twofold copy number gain included up to 20 genes but only the HUWE1 gene is located in the minimal common region of overlap in these families. Moreover, expression analysis revealed about twofold increased HUWE1 mRNA levels in affected patients when compared to control individuals. Breakpoint analysis revealed Non-homologous end-joining (4 cases), serial replication slippage (1 case) and non-allelic homologous recmbination (one case) as the potential recombination mechanism. For duplication mapping and exact copy number analysis in all four families, differentially-labeled patient versus male control DNA samples were hybridized onto a custom designed 4x44k oligo-array (Agilent Technologies) that covers the repeat-masked region 52.50 Mb to 54.50 Mb at tiling resolution.
2012-09-03 | E-GEOD-32945 | biostudies-arrayexpress
Project description:The monkey infecting Helicobacter pylori strain USU101 used in a long term infection of macaques with and without the dietary carcinogen ENNG was analyzed for gene content compared to the sequenced strains 26695 and J99 We performed array CGH using two microarrays to analyze the gene content of the starting strain (USU101) used for the monkey infection experiment (GSE60405). The ENNG information is not relevant.
2014-08-18 | E-GEOD-60404 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2014-08-18 | E-GEOD-60474 | biostudies-arrayexpress
Project description:In a study to elucidate the genetic defects in patients with X-linked mental retardation (XLMR) we performed X chromosome-specific BAC-array-CGH and identified a 0.33 Mb inherited recurrent copy number gain at Xq28 in affected males of four unrelated XLMR families. All aberrations segregate with the disease in the families and the carrier mothers show a nonrandom X-inactivation. Tiling Xq28 region-specific oligo-array revealed that all aberrations start at the same position (153.218 Mb) and end between 153.530 and 154.542 Mb. The copy number gain is complex in nature but always included 18 genes of which three, RPL10, ATP6AP1 and GDI1, are highly expressed in brain. From these, the copy number of GDI1 correlated with the severity of clinical features since it was duplicated in one family with nonsyndromic moderate MR, triplicated in males from two families with mild MR and additional features, while in a fourth family with a severe syndromic form of MR, it was present in four copies. Moreover, expression analysis revealed copy number-dependent increased mRNA levels in affected patients compared to control individuals. Interestingly, the breakpoint junction regions suggested a yet unknown recombination mechanism between two adjacent but different sets of low copy repeats. For duplication mapping and exact copy number analysis in all four families, differentially-labeled patient versus male control DNA samples were hybridized onto a custom designed 4x44k oligo-array (Agilent Technologies) that covers the repeat-masked region 152.70 Mb to 153.65 Mb at tiling resolution.
2010-08-16 | E-GEOD-17813 | biostudies-arrayexpress
Project description:Breast cancer ranks top in the incidence among the main sites of female cancer in Japan. The epidemiological study on atomic bomb survivors has suggested that the excess relative risk for breast cancer is higher than any other sites. Little is known, however, about the molecular mechanisms of breast cancer induction by radiation. Therefore, we analyzed here the genome-wide copy number aberration of radiation-induced rat mammary carcinomas using microarray-based comparative genomic hybridization (array-CGH). Mammary carcinomas were induced by 2 Gy gamma irradiation of Sprague-Dawley (SD) rats at 3 or 7 weeks of age. We examined 14 mammary carcinomas induced by gamma-irradiation (2 Gy) and found 26 aberrations including trisomies of chromosomes 4 and 10 in 3 and 1 carcinomas, respectively, and deletion of chromosomes 3q35q36 and 5q32 (Cdkn2a and Cdkn2b region) in 2 and 2 carcinomas, respectively. On the other hand, only one aberration (amplification of chromosome 10q31) was observed in four spontaneous mammary carcinomas. These results suggest that the trisomy of chromosome 4 and deletion of chromosomes 3q35q36 and 5q32 were associated with radiation exposure. We performed aCGH on mammary carcinoma in Sprague-Dawley rat to identify radiation-specific DNA copy number aberration compared with spontaneous mammary carcinoma.
2010-08-08 | E-GEOD-16128 | biostudies-arrayexpress